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CURRENT SCIENCE REVIEWS    by Joe Bruman   January 1997    P.1 of 2

Klatka L et al; Neur 1996;47:1148-1152:
Retrospective incidence of depression, hallucinations, and
delusions in 28 subjects with Diffuse Lewy Body Disease, 56 with
Alzheimer's Disease, and 28 autopsied Parkinson's patients.

Hillen M, Sage J; Neur 1996;47:1180-1183:
Counted nature and frequency of nonmotor "off" fluctuations
(autonomic, sensory, cognitive/psychiatric) in 130 PD patients
who had motor fluctuations. Modified treatment improved symptoms
in 9 of the 22 who also had nonmotor fluctuations.

Busenbark K et al; Neur 1996;47:1331-1332:
Essential tremor (ET) is the most common movement disorder seen
in clinical practice. Authors tried methazolamide in a controlled
test against voice tremor in 9 patients, but it didn't work.

Taha J et al; J Neurosurg 1996;85:1005-1012:
Authors used microrecording during pallidotomy of 38 patients to
study kinesthetic cells of the globus pallidus.

Fisher N; BMJ 16 Nov 1996:1262 and
O'Sullivan D: BMJ 16 Nov 1996:11262:
Clozapine (Clozaril) is effective against otherwise resistant
schizophrenia, but patients must be monitored for potentially
fatal agranulocytosis. However for black patients the normal
white cell and neutrophil counts may be at or below the alarm
level. Since the incidence of schizophrenia in blacks of the
area studied is four times that in whites, authors suggest
lowering the alarm level to avoid denial of this treatment.

BMJ 23 Nov 1996:1313 (news item):
The gene locus recently found by US workers in a related cohort of
PD patients may be present in only a small fraction of all PWP.

Hawkes, C; BMJ 23 Nov 1996:1278:
Comment on the recent US discovery of a PD gene: 98% of PD patients
have no family history, therefore genetic origin is not certain.

Praamstra P et al; Brain; 1996:119:1689-1704:
Authors compared reaction times with recorded movement-related
potential in a standard task, concluding that preprogramming a
response required more effort by PD patients than by controls.

Elble R et al; Brain 1996;119:1705-1716:
Gait impairment of PD, called lower-half parkinsonism, is caused
by impaired generation of shifts between steady-state postures or
movements.

Guridi J et al; Brain 1996;119:1717-1727:
Nineteen suffering Macaque monkeys, under various regimes of
induced PD and surgery, were used to determine that hyperactivity
of the subthalamic nucleus is paramount in the pathophysiology of
parkinsonism. STN surgery (thalamotomy) confers major improvement
in all features of parkinsonism, except for levodopa-induced
dyskinesia, and authors recommend that it receive more attention.




CURRENT SCIENCE REVIEWS   by Joe Bruman    January 1997  p.2 of 2

Science, 6 December 1996:1612 (news item):
The neurotransmitter glutamate in excess is toxic to neurons.
Researchers in ALS (Lou Gehrig Disease) found in some cases a
genetic defect in the protein that normally neutralizes glutamate.

Tsukada H et al; J Neurosci 1996;16:7670-7677:
Authors dosed rats with cocaine, then measured binding potential
of D1 and D2 dopamine receptor antagonists by high-resolution PET
scan, concluding that binge pattern cocaine may alter availability
of binding sites.

Murphy B et al; J Neurosci 1996;16:7768-7775:
An anxiogenic inverse agonist raises dopamine turnover in the
prefrontal cortex of rats and monkeys but not elsewhere, and the
increased turnover impairs prefrontal-dependent cognitive tasks.
Authors tested various drugs in the ventral tegmental area which
block the increase, and prevented the cognitive deficit, suggesting
that the VTA is an important regulatory site.

Todd R et al; J Neurosci 1996;16:7776-7782:
Authors observed time-dependent changes in D2, D3, and D4 binding
in MPTP-denervated baboons, whose ipsilateral dopamine content was
reduced by over 90%. Over a course of 480 days, Dopamine receptor
binding first decreased, then increased up to 7-fold, then returned
to near baseline levels, suggesting that MPTP-induced changes are
complex.

Cass W; J Neurosci 1996;16;8132-8139:
Chronic methamphetamine intake can induce long-term deficits in
striatal dopamine and serotonin. Since glial cell line-derived
neurotrophic factor (GDNF) can partially protect against MPTP,
authors tried it on rats given methamphetamine. GDNF selectively
protected the dopamine neurons but not the serotonin neurons.

Przedborski S et al; Neur 1996;47:1358-1359:
Perinatal or neonatal hypoxic/ischemic brain injury in rats causes
subsequent loss of striatal dopamine receptors, leading to hemi-
parkinsonism/hemiatrophy. PET scan revealed cortical damage as
well, but PET scan of a human subject with that syndrome showed
no change in striatal dopamine receptors.

Golbe L et al; Ann Neur 1996;40:767-775:
Further statistical analysis of the large Italian-American family
with 60 PD members reinforced autosomal dominance, but with wide
variation in age at onset (20-85yr) and in duration of survival
after onset (2-20yr).

Sanchez-Ramos J et al; Arch Neur 1996;53:1265-1268:
Up to 1/3 of PD patients in long-term treatment may hallucinate.
Questionnaire interviews of 214 routine clinical visitors found
55 who complained of hallucinations related to PD.


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